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Targeting hydrogen sulfide as a promising therapeutic strategy for atherosclerosis.
Int J Cardiol. 2014 Mar 15; 172(2):313-7.IJ

Abstract

Physiological concentrations of nitric oxide (NO) and carbon monoxide (CO) have multiple protective effects in the cardiovascular system. Recent studies have implicated hydrogen sulfide (H2S) as a new member of vasculoprotective gasotransmitter family, behaving similarly to NO and CO. H2S has been demonstrated to inhibit multiple key aspects of atherosclerosis, including atherogenic modification of LDL, monocytes adhesion to the endothelial cells, macrophage-derived foam cell formation and inflammation, smooth muscle cell proliferation, neointimal hyperplasia, vascular calcification, and thrombogenesis. H2S also decreases plasma homocysteine levels in experimental animal models. In the human body, H2S production is predominantly catalyzed by cystathionine-β-synthase (CBS) and cystathionine γ-lyase (CSE). CSE is the primary H2S-producing enzyme in the vasculature. Growing evidence suggests that atherosclerosis is associated with vascular CSE/H2S deficiency and that H2S supplementation by exogenous H2S donors (such as NaHS and GYY4137) attenuates, and H2S synthesis suppression by inhibitors (such as D, L-propargylglycine) aggravates the development of atherosclerotic plaques. However, it remains elusive whether CSE deficiency plays a causative role in atherosclerosis. A recent study (Circulation. 2013; 127: 2523-2534) demonstrates that decreased endogenous H2S production by CSE genetic deletion accelerates atherosclerosis in athero-prone ApoE-/- mice, pinpointing that endogenously produced H2S by CSE activation may be of benefit in the prevention and treatment of atherosclerosis. This study will facilitate the development of H2S-based pharmaceuticals with therapeutic applications in atherosclerosis-related cardiovascular diseases.

Authors+Show Affiliations

Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China; Cardiovascular and Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1590, USA. Electronic address: suowen.xu@gmail.com.Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China. Electronic address: liupq@mail.sysu.edu.cn.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

24491853

Citation

Xu, Suowen, et al. "Targeting Hydrogen Sulfide as a Promising Therapeutic Strategy for Atherosclerosis." International Journal of Cardiology, vol. 172, no. 2, 2014, pp. 313-7.
Xu S, Liu Z, Liu P. Targeting hydrogen sulfide as a promising therapeutic strategy for atherosclerosis. Int J Cardiol. 2014;172(2):313-7.
Xu, S., Liu, Z., & Liu, P. (2014). Targeting hydrogen sulfide as a promising therapeutic strategy for atherosclerosis. International Journal of Cardiology, 172(2), 313-7. https://doi.org/10.1016/j.ijcard.2014.01.068
Xu S, Liu Z, Liu P. Targeting Hydrogen Sulfide as a Promising Therapeutic Strategy for Atherosclerosis. Int J Cardiol. 2014 Mar 15;172(2):313-7. PubMed PMID: 24491853.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Targeting hydrogen sulfide as a promising therapeutic strategy for atherosclerosis. AU - Xu,Suowen, AU - Liu,Zhiping, AU - Liu,Peiqing, Y1 - 2014/01/24/ PY - 2013/08/09/received PY - 2014/01/02/revised PY - 2014/01/18/accepted PY - 2014/2/5/entrez PY - 2014/2/5/pubmed PY - 2015/1/13/medline KW - Atherosclerosis KW - Cystathionine γ-lyase KW - Gasotransmitter KW - Hydrogen sulfide SP - 313 EP - 7 JF - International journal of cardiology JO - Int J Cardiol VL - 172 IS - 2 N2 - Physiological concentrations of nitric oxide (NO) and carbon monoxide (CO) have multiple protective effects in the cardiovascular system. Recent studies have implicated hydrogen sulfide (H2S) as a new member of vasculoprotective gasotransmitter family, behaving similarly to NO and CO. H2S has been demonstrated to inhibit multiple key aspects of atherosclerosis, including atherogenic modification of LDL, monocytes adhesion to the endothelial cells, macrophage-derived foam cell formation and inflammation, smooth muscle cell proliferation, neointimal hyperplasia, vascular calcification, and thrombogenesis. H2S also decreases plasma homocysteine levels in experimental animal models. In the human body, H2S production is predominantly catalyzed by cystathionine-β-synthase (CBS) and cystathionine γ-lyase (CSE). CSE is the primary H2S-producing enzyme in the vasculature. Growing evidence suggests that atherosclerosis is associated with vascular CSE/H2S deficiency and that H2S supplementation by exogenous H2S donors (such as NaHS and GYY4137) attenuates, and H2S synthesis suppression by inhibitors (such as D, L-propargylglycine) aggravates the development of atherosclerotic plaques. However, it remains elusive whether CSE deficiency plays a causative role in atherosclerosis. A recent study (Circulation. 2013; 127: 2523-2534) demonstrates that decreased endogenous H2S production by CSE genetic deletion accelerates atherosclerosis in athero-prone ApoE-/- mice, pinpointing that endogenously produced H2S by CSE activation may be of benefit in the prevention and treatment of atherosclerosis. This study will facilitate the development of H2S-based pharmaceuticals with therapeutic applications in atherosclerosis-related cardiovascular diseases. SN - 1874-1754 UR - https://www.unboundmedicine.com/medline/citation/24491853/Targeting_hydrogen_sulfide_as_a_promising_therapeutic_strategy_for_atherosclerosis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0167-5273(14)00277-0 DB - PRIME DP - Unbound Medicine ER -